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Resnik-Docampo et al. demonstrate that depletion of the tricellular junction protein Gliotactin in young flies leads to hallmarks of ageing, including an increase in intestinal stem cell proliferation and a block in terminal differentiation.
Daley and colleagues report that MAPK signalling controls pluripotency in embryonic stem cells and during somatic cell reprogramming by enhancing the stability and effects of LIN28 on direct mRNA targets through its phosphorylation by ERK.
Ly et al. establish a method to selectively inactivate the centromere of the Y chromosome to follow chromosome shattering and micronuclei formation through several cell cycles, and suggest re-ligation of chromosome fragments is dependent on non-homologous end joining.
Hansen et al. find that SCAI (suppressor of cancer cell invasion) is a 53BP1-binding protein that acts to repair in heterochromatin and to facilitate meiotic recombination in germ cells.
By modulating the presence of lamellipodia and filopodia, Sixt and colleagues determine that migrating dendritic cells rely on these protrusions for directed migration in complex environments, whereas locomotion per se is not driven by lamellipodia.
Muthuswamy et al. report that in macrophages SCRIB interacts with the NADPH oxidase complex to promote the production of reactive oxygen species needed to kill bacteria. Conversely, loss of SCRIB promotes M1 macrophage polarization and inflammation.
Guesdon et al. characterize the microtubule-end-binding region of EB1 using cryo-electron tomography, providing insights into the mechanism of this interaction and the architectural changes in the GTP-cap region during microtubule growth.
It has been unclear how the relatively weak dynein motor can counterbalance kinesin forces during microtubule-dependent transport. Belyy et al. find that binding of dynactin and BICD2 increases the strength of the dynein motor.
By engineering mice to express a version of the Pten tumour suppressor that lacks the three C-terminal amino acids, van Deursen and colleagues reveal a role for the protein in the generation of symmetric spindles through recruitment of Eg5 to centrosomes.
Pollard and colleagues demonstrate in vitro and in fission yeast that the LifeAct actin probe can affect actin filament nucleation and dynamics and perturb actin-dependent cellular processes unless low concentrations are used.
Chromosome missegregation can lead to p53 activation to block proliferation of aneuploid cells. Hinchcliffe, Dong and colleagues find that generation and spreading of a histone H3.3 Ser31 phosphorylation mark mediates this response.
The imaging of individually labelled sister chromatids allows Nagasaka et al. to conclude that mitotic sister chromatin resolution begins in prophase and depends on the activity of topoisomerase II and condensin II, but not on cohesin dissociation.
Costanzo and colleagues find, by reconstitution of repetitive centromeric DNA replication in Xenopus egg extracts, that replication is facilitated by suppression of ATR-mediated checkpoint signalling and formation of DNA loop structures.
Lien et al. show that oncogenic PI(3)K/Akt signalling stimulates glutathione (GSH) synthesis by activation of the transcription factor Nrf2 and regulation of GSH biosynthesis genes in breast cancer.
Vincent and colleagues show in Drosophila wing imaginal discs that the signalling molecule Wingless is synthesized and secreted at the apical surface, and is re-internalized to be transcytosed basally, where its signalling occurs.
Using live imaging of zebrafish angiogenesis, Gerhardt and colleagues observe blood-flow-regulated inverse membrane blebbing during lumen expansion, and show that actomyosin contractility is needed for both bleb retraction and lumen formation.
Kornfeld and colleagues identify miRNAs that are dysregulated in brown adipose tissue in mouse models of obesity and ageing, and show that miR-328 targets Bace1 to promote brown adipogenesis.
By culturing rat hepatocyte doublets in microwells with controlled ECM environments, Viasnoff and colleagues show that the lumen between the cells extends anisotropically towards regions of lower intercellular tension.
By proteomics analysis of conditioned media from cells with constitutive mTORC1 activity, Yu and colleagues identify IGF binding protein 5 (IGFBP5) as a protein that is induced by mTORC1 through HIF1 and that blocks IGF-1 signalling.
Eichel et al. show that β-arrestin-mediated MAPK activation by GPCRs involves dissociation of β-arrestin from its activating GPCR, and accumulation of β-arrestin in clathrin-coated structures, where it promotes MAPK signalling.